(1/137) Serum dilution neutralization test for California group virus identification and serology.

The serum dilution neutralization test was evaluated for serological diagnosis of California group arbovirus infections and identification of virus isolates. The technical advantages and the degree of subtype specificity of the serum dilution neutralization test over the hemagglutination inhibition test and the complement fixation test were demonstrated with paired specimens from human cases, single human survey sera, and sentinel rabbit sera. Twenty-one virus isolates from various geographical areas of the United States were also used to evaluate the efficacy of the serum dilution neutralization test for specific virus identification.  (+info)

(2/137) Light-independent inactivation of dengue-2 virus by carboxyfullerene C3 isomer.

Carboxyfullerene (C60) is known as a photosensitizer for virus inactivation. Its regioisomer with C3 symmetry, named the C3 isomer, could also inactivate the dengue-2 virus without light when the dose of C3 isomer was increased to 40 microM, indicating the possible involvement of a light-independent mechanism. Further analysis showed that the C3 isomer blocked viral replication at the attachment and penetration stages, suggesting that a direct interaction between the C3 isomer and the virion is required for inactivation. The C3 isomer with a bipolar structure showed better lipid interaction and dengue-2 virus suppression than D3, another isomer that contains evenly distributed hydrophilic side chains. Moreover, the C3 isomer selectively inactivated enveloped viruses (viz., dengue-2 virus and Japanese encephalitis virus) instead of nonenveloped viruses (viz., enterovirus 71 and coxsackievirus B3). Collectively, these findings support the hypothesis that C3 isomer suppression of enveloped viruses is effected through its hydrophobic interaction with the viral lipid envelope. Our report, which demonstrates the light-dependent and -independent mechanisms of C60 on viral inactivation, will aid in the development of novel anti-viral agents for use against enveloped viruses.  (+info)

(3/137) Intrauterine infection of mice with St. Louis encephalitis virus: immunological, physiological, neurological, and behavioral effects on progeny.

Intravenous injection of pregnant mice with St. Louis encephalitis (SLE) virus at 8 days of gestation resulted in infection of the fetus. Progeny developed no antibody or tolerance to SLE virus since the viral antigen was cleared by maternal antibody before antibody-forming competence developed in the young. Temporary growth retardation was observed in a number of young at 3 weeks of age. After the initial setback the growth rate increased, indicating that early runting was due to an inability to adjust adequately to extrauterine life, which was subsequently overcome. In most other young there were no significant effects on growth, reproduction, or life expectancy. A few young died at or shortly after birth; in these, neurological changes ranging from gross defects such as encephaloceles and hydrocephalus to histological evidence of necrosis and congestion were observed. Neurologically related behavioral changes were detected by using the open field test and the rotating-rod test, which indicated neurological damage and memory impairment in the surviving intrauterinely infected animals.  (+info)

(4/137) Viral encephalitis in England, 1989-1998: what did we miss?

We analyzed hospitalizations in England from April 1, 1989, to March 31, 1998, and identified approximately 700 cases, 46 fatal, from viral encephalitis that occurred during each year; most (60%) were of unknown etiology. Of cases with a diagnosis, the largest proportion was herpes simplex encephalitis. Using normal and Poisson regression, we identified six possible clusters of unknown etiology. Over 75% of hospitalizations are not reported through the routine laboratory and clinical notification systems, resulting in underdiagnosis of viral encephalitis in England. Current surveillance greatly underascertains incidence of the disease and existence of clusters; in general, outbreaks are undetected. Surveillance systems must be adapted to detect major changes in epidemiology so that timely control measures can be implemented.  (+info)

(5/137) Solid-phase radioimmunoassay for antibodies to flavivirus structural and nonstructural proteins.

A micro-solid-phase radioimmunoassay (SPRIA) is described for quantitation of antibodies to purified flaviviruses as well as to the purified envelope glycoprotein and 80,000-molecular-weight viral nonstructural protein. Sera from mice experimentally infected with Saint Louis encephalitis (SLE) virus or from humans after a primary SLE virus infection reacted more specifically with the major viral envelope protein in the SPRIA test than with antigens conventionally used in the complement fixation (CF) and hemagglutination inhibition tests. A high degree of correlation (P is less than 0.05) was observed between SPRIA anti-immunoglobulin G binding values with the 80,000-molecular-weight nonstructural protein of SLE virus and antibody titers obtained by plaque reduction neutralization and CF with the nonstructural protein. In five of seven human sera in which CF antibody titers to the nonstructural protein were 4 or less, SPRIA testing revealed significant titers of IgG immunoglobulin reactive with this viral protein. The SPRIA test for antibodies reactive with group B togavirus nonstructural protein is as specific and sensitive as the plaque reduction neutralization test for titrating viral antibody in human and animal sera. Antibodies reactive with viral envelope proteins are broadly cross-reactive by the Spria technique, demonstrating both group- and complex-reactive antigenic determinants. The SPRIA test, using wells precoated with antigen, can be completed in 1 day, providing a rapid, highly sensitive test which can be adapted to use in testing a large number of sera.  (+info)

(6/137) Powassan and Silverwater viruses: ecology of two Ontario arboviruses.

Powassan virus was isolated from a pool of Ixodes marxi ticks collected during late August 1962, from a red squirrel, Tamiasciurus hudsonicus, and from blood obtained from a red squirrel during early October 1962 near Powassan, Ontario, where a child contracted fatal encephalitis due to this virus in September 1958. The frequent detection of Powassan virus neutralizing antibody in sera of squirrels captured during autumn, but rarely at other seasons, and the frequent I. marxi infestation of squirrels, some of which contain antibody, but the lack of occurrence of I. marxi on other forest rodents, suggest that I. marxi ticks are vectors and squirrels are reservoirs of Powassan virus infection. Isolation of Silverwater virus from Haemaphysalis leporis-palustris ticks which infested a snowshoe hare Lepus americanus near Powassan demonstrates the presence of this agent in the Powassan area also.  (+info)


Lockart, Royce Z., Jr. (The University of Texas, Austin). Production of an interferon by L cells infected with Western equine encephalomyelitis virus. J. Bacteriol. 85:556-566. 1963.-Two strains of Western equine encephalomyelitis virus (WEE), WEE (L+) and WEE (L-), which differed with respect to their cytopathogenicity for L cells were isolated. Both strains reproduced in L cells, and both induced the production of an interferon distinct from virus particles. L-cell monolayers were protected from degeneration by prior addition of interferon. By use of the absence of cytopathic effects (CPE) as an end point, interferon content was assayed. Monolayers failing to show CPE consistently produced less than 2% as much virus as control monolayers, indicating that virus synthesis was also inhibited. The use of this assay method was facilitated by the use of horse serum that appeared to contain antibodies against WEE and that permitted interferon to act selectively in the presence of active virus. It was found that interferon was produced during the time in which active virus was produced, and not significantly later. No interferon could be found in fluids from cells treated with inactive virus, although these are known to act as interfering agents. Interferon production was inhibited by pretreatment of L cells with sufficient amounts of interferon. It is concluded that interferon production is closely connected with WEE virus synthesis in L cells. The question is raised as to whether interferon need be a necessary intermediate for interference in L cells.  (+info)


More than 150 arthropod-borne viruses are now recognized, and over 50 of these are known to produce human infections and disease. Among these viruses are those of the tick-borne Russian spring-summer complex, which is etiologically involved in a wide variety of human diseases of varying severity. The eight antigenically different members of this complex so far known are Russian spring-summer encephalitis, louping-ill, Central European encephalitis, Omsk haemorrhagic fever, Kyasanur Forest disease, Langat, Negishi and Powassan viruses.In his review of the problems posed by these viruses and of research on them, the author points out that, while this complex is distributed around the globe in the temperate zone of the northern hemisphere, the only serious tick-borne virus disease known in the tropics is Kyasanur Forest disease. It is probable, however, that there are other, unrecognized tick-borne viruses in the tropical areas of Asia, Africa and America of importance to human health, and that these will be brought to light as virological studies of diseases of now obscure etiology are pursued.  (+info)